The general anesthetics depress most excitable cells. They induce anesthesia in the central nervous system, and depress transmission across ganglionic synapses. The effect on ganglionic transmission appears to involve actions at both presynaptic and postsynaptic sites. The mechanisms of these actions will be explored. Electrophysiological techniques will be used to analyze the effects of halotane and other general anesthetics on the hamster stellate ganglion. Changes in the e.p.s.p. (excitatory postsynaptic potential) and slow e.p.s.p. recorded from single cells with microelectrodes will be related to alterations of presynaptic or postsynaptic events. The effect of halothane on the release of transmitter will be described by observing the changes in quantal release from the nerve endings and in the action potentials of the nerve endings. Postsynaptic actions of halothane will be related to effects on the postsynaptic receptors, the postsynaptic conductance changes, or the non-synaptic membrane. Concurrently, the effects of anesthetics on inhibition in the ganglion will be explored with the sucrose-gap technique. With these experiments it should be possible to describe the basic mechanisms by which halothane affects ganglionic transmission. Postganglionic recording methods will be used to compare many general anesthetics to decide whether all anestetics act by the same basic mechanism or whether the variation in chemical structure of anesthetics is accompanied by a variation in the mechanism of production of blockade.